PubMed · 4701800
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G P Lewis, L L Coughlin. 1973. Wet ashing using a closed system.. https://doi.org/10.1136/jcp.26.4.311
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For analysis of monoclonal antibodies using polyacrylamide gel electrophoresis, two hydrolytic fragments derived from the heavy chain of mouse IgG1 were produced during incubation of the antibodies in Laemmli reducing sample buffer at 100 degrees C for 5 min. The cleavage sites were identified by amino terminal sequencing. Results indicate that the final pH of the mixture is critical for the production of the fragments which are generated when the pH is approximately 6.0. At pH 8.0, no fragments are detected. The relevance of this finding to those working with monoclonal antibodies is discussed.
Recent observations using both clinical and animal models have suggested that acidosis may initiate pain and sensitization. In the present study, we examined if changing the acidic environment around the rat sciatic nerve resulted in thermal hyperalgesia. Fresh solutions of preservative-free saline (PFS) and unbuffered PFS acidified to pH 3.5 were continuously infused around the left rat sciatic nerve for 7 days. Rats receiving unbuffered, acidified PFS developed a progressive thermal hyperalgesia that was maximal on infusion day 6. Unbuffered, acidified PFS significantly decreased the perineural pH (pH 6.9 +/- 0.15, P < 0.05), and decreasing perineural pH values were significantly correlated with increasing thermal hyperalgesia (r = 0.91) for individual rats. While it is likely that multiple factors play a role in the development of neuropathic pain, these data demonstrate that an acidic environment around the sciatic nerve will produce thermal hyperalgesia.
1. Chicken enterocytes present a Na(+)-independent proton transport mechanism involved in pHi recovery from an acid load. In the current study the nature of this proton transport system is investigated. 2. The pHi of acid-loaded cells increased when transferred to Na(+)-free, pH 7.4 buffers, both at 6 and 65 mM extracellular potassium concentration. Addition of nigericin accelerated the rate of cell alkalinization. 3. When acid-loaded cells were transferred to a Na(+)-free, pH 6.5 buffer, the cells acidified further, regardless of the extracellular potassium concentration. The addition of nigericin increased the rate of acidification at 6 mM K+ but produced an alkalinization at 65 mM K+. 4. The rate of the Na(+)-independent regulatory cell alkalinization was inhibited by SCH 28080, DCCD, NBD-Cl, rotenone or Zn2+. Addition of valinomycin reversed the inhibition induced by SCH 28080, DCCD and NBD-Cl but not that induced by Zn2+ or rotenone. Zn2+ inhibition was abolished by the metal chelator DTPA. 5. Cytosolic acidification increased the rate of Na(+)-independent regulatory cell alkalinization. 6. The results suggest that the Na(+)-independent proton transport system is a Zn(2+)-sensitive proton-conducting pathway which is regulated by the cytosolic proton concentration.